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BEACON MedSurg/Peds > Alterations in mobility Test 4 > Flashcards

Alterations in mobility Test 4 Flashcards

1
Q

Static encephalopathy

A

cerebral palsy

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2
Q

Brain injury that is a non-progressive disorder of posture and movement

A

Encephalopathy

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3
Q

most common type of cerebral palsy

A

rigid-spastic

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4
Q

Often associated with epilepsy, speech problems, vision compromise, & cognitive dysfunction

A

cerebral palsy

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5
Q

issues with balance and coordination. Problems with depth perception

A

ataxic

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6
Q

very unique abnormal movement. Writhing. Can effect hands, feet, tongue thrusting, often times there are challenges in feeding

A

athetoid

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7
Q

have severely decreased motor tone. Kind of like rag dolls

A

atonic

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8
Q

combination of two or more of the different types of cerebral palsy

A

mixed (usuallty rigid-spastic with the athetoid)

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9
Q

Hemiplegic

A

one side of the body is affected

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10
Q

triplegic

A

three sides of the body are affected

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11
Q

Diplegic

A

all four extremities are effected, but lower extremities are more affected than the upper

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12
Q

most common topographic presentation of cerebral palsy

A

diplegic

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13
Q

Infection, anoxia, toxic, vascular, Rh disease, genetic, congenital malformation of brain

A

Prenatal etiology of cerebral palsy

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14
Q

anoxia, traumatic delivery, metabolic

A

natal etiology of cerebral palsy

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15
Q

Big concern of infection in prenatal women as far as cerebral palsy

A

Ruebella

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16
Q

Trauma, infection, toxic etiology

A

Post natal etiology of cerebral palsy

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17
Q

Could cause baby to develop athetoid cerebral palsy

A

Severe jaundice

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18
Q

A risk factor for development of cerebral palsy

A

prematurity

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19
Q
  • Persistent primitive reflexes
  • Poor head control after afe 3 months
  • Stiff or rigid limbs
  • Arching back, pushing away
  • Floppy tone
  • Unable to sit without support at age 8 months
  • Clenched fists after age 3 months
A

Possible motor signs of CP

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20
Q
  • Excessive irritability
  • No smiling by age 3 months
  • Feeding difficulties
                     - Persistent tongue thrusting
                 - Frequent gagging or choking with feedings
A

Possible behavioral signs of Cerebral Palsy

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21
Q
  • Establish locomotion, communication, and self-help skills
  • Gain an optimal appearance and integration of motor functions
  • Correct associated defects as effectively as possible
  • Provide adapted educational opportunities
  • Promote socialization experiences with other affected and unaffected children
A

Therapeutic Nursing Goals for individuals with CP

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22
Q
  • Spasticity
  • Weakness
  • Increase reflexes
  • Clonus
  • Seizures
  • Articulation & Swallowing difficulty
  • Visual compromise
  • Deformation
  • Hip dislocation
  • Kyphoscoliosis
  • Constipation
  • Urinary tract infection
A

CP complications

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23
Q

Management of Cerebral Palsy (5)

A
  • Promote growth and development
  • OT and PT
  • Speech
  • Adaptive equipment
  • Surgical
  • Rhizotomy, Baclofen pumps, Botoxin
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24
Q

What is substantially disabling Cerebral Palsy

A
  • Mobility
  • Communication
  • Learning
  • Self Care
  • Self Direction
  • Independent Living
  • Economic Sufficiency
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25
Q

Surgery where they cut nerves very close to where they’re coming off the spinal cord

A

Rhizotomy

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26
Q

Baclofen pump

A

Continuous infusion of baclofen intrathecally to decrese the spacicity

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27
Q
  • Defects of closure of neural tube during fetal development
  • Congenital (present at birth)
  • Believed to be caused by genetic or environmental factors, but exact etiology is unknown
A

Neural tube disorders: one of the most common neural defects

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28
Q

Common in women with poor folic acid intake before and during pregnancy

A

Neural tube defects

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29
Q
  • Not visible externally
  • Lamina fail to close but spinal cord does NOT herniate or protrude through the defect
  • No motor or sensory defects
  • Tuft of hair
A

Spina Bifida occulta

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30
Q
  • External sac that contains meninges and CSF
  • Protrudes through defect in vertebral column
  • Not associated with neurologic deficit – good prognosis
  • Hydrocephalus may be an associated finding, or aggravated after repair (large heads)
A

Spina Bifida Meningocele

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31
Q
  • Same as above, but the spinal cord and meninges protrude through the defect in the bony rings of the spinal cord
  • Contains nerves therefore the infant will have motor and sensory deficits below the lesion
  • Visible at birth, most often in the lumbaosacral area
  • Covered with a very fragile thin membrane/sac which can tear easily, allowing CSF to leak out
A

Spina Bifida Cystica Myelomeningocele

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32
Q

Three areas we focus on for nursing interventions for neural tube defects

A
  • Protect the sac from injury
  • Keep free from infection: Position: prone or side lying. Cover sac with sterile, moist non-adherent dressing, sterile technique imperative
  • Parents need emotional support & education regarding short and long term needs of infant
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33
Q

When does surgical repair occur with neural tube defects?

A

Within the first 24 hours

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34
Q

What to look for after neural tube defect surgery?

A

observe for early signs of infection: elevated temp, irritability, lethargy, nuchal rigidity
observe for signs of increasing ICP (may indicate hydrocephalus)

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35
Q
  • Degeneration of skeletal muscle fibers: undergoes necrosis and replacement with fat. Loss of muscle mass is progressive.
  • Duchenne’s
  • Becker’s
  • Facioscapulohumeral
  • Scapluloperoneal
  • Limb Girdle
A

Muscular Dystrophy

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36
Q
  • X-linked disorder
  • Etiology: Genetic defect
                - Defective dystrophin protein (need it for   attachment of skeletal muscles to attachment of the basement membrane that attaches to surrounding bone tissue
  • Most common type
A

Duchene’s Muscula Dystrophy

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37
Q

Weak muscle attachment
↓
Fiber tearing with repeated use
↓
Muscle cell regeneration (initially) produces more defective cells
Later - muscle necrosis–>Replacement with adipose and fibrous tissue

A

Pathogenesis of Duchene’s Muscular Dystrophy

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38
Q

Postural muscles in the hips & shoulders affected

  • Frequent falling

*Age?

A

Age 3-5 for DMD clinical manifestation

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39
Q
  1. Imbalances between agonist and antagonist muscle groups
  • Kyphoscoliosis, contractures & joint immobility
  • Wheelchair dependent
  • Cardiomyopathy

*age?

A

Age 7-12 DMD clinical manifestations

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40
Q

Which disorder?

A

Changes seen with DMD

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41
Q

Kyphoscoliosis

A

Being an abnormality in terms of skeletal structure. Posterior spine being changed in terms of the normal curvatures. Exaggerated thoracic and lateral curve

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42
Q
  • ↓ depth of respiration–>Hypercapnea
  • (increased PaCO2)
  • hypoxemia (↓ PaO2)
  • ineffective cough
  • Decreased clearance of secretions
A

Effects of Kyphoscoliosis

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43
Q

Diagnosis of kyphoscoliosis

A
  • physical assessment
  • Elevated creatine kinase (CK): serum blood test for damage to muscles
  • muscle biopsy
  • DNA testing
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44
Q

Complications of kyphoscoliosis

A

recurrent respiratory infections

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45
Q

Causes of death related to kyphoscoliosis

A
  • Heart failure
  • Respiratory Failure
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46
Q
  1. Demyelinated plaques in white matter of the central nervous system
  2. Etiology
  • Genetic predisposition
  • Northern European decent, twice as common in women than men in 20-30s
    1. Precipitating event: pregnancy, stress, consequence following a viral infection
A

Multiple Sclerosis

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47
Q
  • ? immune mediated
  • Macrophage, CD4 & CD8 cell invasion of plaques
  • Injury to Oligodendrocytes ——>demyelination –>degeneration of the nerve
  • Slowed conduction at first
  • Blocked impulse conduction later
A

MS pathogenesis

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48
Q
  • Changes in visual fields
  • Abnormal gait
  • Bladder and sexual dysfunction
  • Vertigo
  • Nystagmus
  • Fatigue
  • Speech problems
  • Paresthesias: numbness, tingling, burning sensation
  • Psychological symptoms
A

Clinical manifestations of MS

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49
Q
  • Shakiness, difficulty walking
  • Fatigue, muscle weakness
  • Numbness, tingling
  • Tinnitus
  • Visual problems
  • Difficulty chewing and speaking
  • Incontinent; impotent

*subjective or objective s/s of MS

A

Subjective

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50
Q
  • Ataxia
  • Changes in behavior & emotions
  • Nystagmus
  • Spasticity, tremors, dysphagia, facial palsy, speech impaired, fatigue
  • Urinary Incontinence
  • Impaired judgment

*subjective/objective s/s of MS?

A

objective

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51
Q

Relapsing-remitting of clinical course of MS

A

Clear relapses with complete or partial recovery, no progression between “attacks”

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52
Q

Primary progressive clinical course of MS

A

Steady progression with plateaus or minor improvements

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53
Q

Secondary progressive course of MS

A

Early relapses and recovery with later progression between “attacks”

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54
Q

Progressive-relapsing clinical course of MS

A

Steadily progressive aggravated by acute attacks

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55
Q

Pharm management of MS

A
  1. Corticosteroids (given during an attack or exacerbation): ACTH, Solu Medrol, Prednisone
  2. Muscle Relaxants: Baclofen, Dantrolene (muscles of the bladder), Valium
  3. I_mmunosuppressants (given during an attack or exacerbation)_: Imuran, Cytoxan
  4. Immunomodulators: Avonex, Betaseron, Copaxone
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56
Q
  1. Degeneration of the basal ganglia of the substantia nigra
  2. Etiology
  • Primary: really don’t know why they have itidiopathic
  • Secondary: Trauma, infection, Drugs,Toxins
A

Parkinsons disease

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57
Q
  • Degeneration of the dopaminergic pathways
  • Loss of basal ganglia dopamine receptors
A

Parkinsons disease pathways

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58
Q

Cardinal symptoms of Parkinsons disease

A
  • Tremors: pill rolling
  • Rigidity
  • Akinesis or bradykinesis: shuffling
  • Postural abnormalities: mask-like facial appearance
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59
Q

Clinical course of Parkinson’s disease

A
  • insidious onset
  • slow progression of symptoms
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60
Q

Pharm management of Parkinson’s disease

A
  1. Dopaminergics: levodopa, sinemet, symmetrel
  2. Dopamine agonists: Parlodel, Permax, Mirapex, Requip
  3. Anticholinergics (controlling drooling, tremors, rigidity): Artane, Cogentin, Parsidol, Akineton
  4. Monoamine Oxidase Inhibitors: Eldepryl (selegiline)
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61
Q
  • Defect in nerve impulse conduction at the neuromuscular junction
  • Etiology: autoimmune disorder,
  1. acetylcholine receptor antibody (Ach-R IgG)
  2. More common in women
  3. Thyoma or Thymic hyperplasia
  • More likely diagnosed in young to middle adulthood
A

Myasthenia Gravis

62
Q
  • Blockage and gradual destruction of Ach-R
  • Low amplitude end plate potential
  • Weak muscle contraction
A

Myasthenia Gravis pathogenesis

63
Q

Initial signs and symptoms of myasthenia gravis

A
  • diplopia
  • ptosis
64
Q

Tremors at rest, tremor decreases or goes away with intentional activity

A

Parkinson’s disease

65
Q
  • Huge complication we’re worried about in Myasthenia Gravis
A

Difficulty swallowing leading to respiratory insufficiency

66
Q
  • History and physical
  • Nerve stimulation tests
  • Presence of the Ach-R IgG
  • Tensilon test: IV edrophonium chloride (Tensilon®) → improvement in muscle weakness
A

Myasthenia gravis dx

67
Q
  • Too little acetylcholine
  • Infection
  • Exacerbation of MG symptoms
  • Respiratory arrest
  • **TENSILON TEST TO DISTINGUISH

*type of myasthenia complication

A

Myasthenia Crisis

68
Q
  • Too much acetylcholine
  • Excess medication
  • Sudden extreme weakness
  • Respiratory arrest

*type of myasthenia complication

A

Cholinergic crisis

69
Q

Myasthenia Gravis medication and other procedure management

A
  • Anticholinesterases: Mestinon, Prostigmin, Mytelase
  • Immunsuppressives: Prednisone, Imuran
  • Other Procedures: Plasmapheresis (filter the blood to remove antibodies that are destroying acetylcholine), Thymectomy (removal of the thymus, may take several years before full effects are experienced)
70
Q

Factors in exacerbation in Myasthenia Gravis?—infection, stress, surgery, hard physical exercise, sedatives, enemas, strong cathartics
Avoid overheating, crowds, overeating, erratic changes in sleeping habits, emotional extremes

A
  • infection, stress, surgery, hard physical exercise, sedatives, enemas, strong cathartics

Avoid overheating, crowds, overeating, erratic changes in sleeping habits, emotional extremes

71
Q
  • No muscle nutrition
  • Lou Gehrig’s disease
  • Destruction of upper and lower motor neurons
           - Anterior horn cells (LMN)
        - Motor nuclei (brain stem)
        - Cerebral cortex motor neurons (UMN)
  • Amyotrophy: atrophy of muscles that hardens tissues of the spinal cord in the lateral column
  • 50-60 years of age, usually men. Lifespan is usally 2-5 years
A

Amyotrophic lateral sclerosis

72
Q
  • muscle weakness and atrophy that leads to a flacid quadriplegia
  • Atrophy of tongue, facial muscles
  • Fasciculations: localized twitching
A

Amyotrophic lateral sclerosis

73
Q

Famous scientist with Atrophic lateral sclerosis

A

Stephen Hawking

74
Q

Diagnosis of amyotrophic lateral sclerosis

A
  • EMG: differentiates neuropathy with myelopathy
  • Muscle biopsy: demonstrates atrophy and loss of muscle fiber
  • Medication: Rilutek (riluzole)
75
Q
  • Autosomal dominant
  • Chromosome 4
  • Clinical onset = 30 to 50 years of age
  • Progressive
  • Fatal within 15 - 20 years
A

Huntington’s Disease

76
Q
  1. Early motor effects of Huntington’s disease early or late?
  • Restlessness
  • Fidgety feeling
  • Minor gait changes
  • Posture disturbances
  • Positioning disturbances
  • Protruding tongue
  • Slurred speech
A

Early motor effects of huntington’s disease

77
Q
  1. Early motor effects of Huntington’s disease early or late?
  • Chorea
  • Facial grimacing
  • Dysphagia
  • Unintelligible speech
  • Impaired diaphragmatic movement
A

Late effects of huntington’s disease

78
Q
  1. Early or late psychosocial clinical manifestations of Huntington’s disease?
  • Irritability
  • Outbursts
  • Depression
  • Risk for suicide
A

Early psychosocial clinical manifestations of Huntington’s disease

79
Q
  1. Early or late psychosocial clinical manifestations of Huntington’s disease?
  • Decreasing memory
  • Loss of cognitive skills
  • Dementia
  • Total dependence
A

Late psychosocial clinical manifestations of Huntington’s disease

80
Q

Medications for Huntington’s disease

A
  • antipsychotics
  • antidepressants
81
Q
  • Acute inflammatory polyneuropathy resulting in demyelination of peripheral nerves
  • Precipitating infection: Campylobacter jejuni, Cytomegalovirus, Mycoplasma pneumoniae
  • CAN recover from this
A

Guillian-Barre Syndrome

82
Q

Macrophage destruction of peripheral nerve myelin
↓
Demyelination
↓
Blocked impulse conduction

A

Guillien-Barre Patho

83
Q

Clinical manifestations of Guillien-Barre syndrome regarding paralysis and autonomic nervous system

A
  • ASCENDING paralysis and paresis: Rapid progression from lower extremity symptoms to paralysis of respiratory muscles
  • Autonomic nervous system dysfunction: Tachycardia or bradycardia. Hyper or hypotension, Facial flushing, Excessive sweating
84
Q
  • Paresthesias
  • Weakness of lower extremities
  • Gradual progressive weakness of upper extremities & facial muscles
  • Possible respiratory failure / arrest
A

Clinical manifestations of Guillain-Barre

85
Q

DX of Guillain-Barre

A
  • Physical exam and history
  • CSF analysis: increased proteins
  • EMG studies: nerve conduction decreased
  • Nerve biopsy: visualize demyelination of peripheral nerves
86
Q

Medication, Other proceedures and treatments of Guillain-Barre syndrome

A
  • Medications: Analgesics, Antibiiotics, Anticoagulants, Vasopressors
  • Other Procedures: Tracheostomy, Plasmaphoresis
  • PT / OT
87
Q

Long bones are _____ and ______ dense and can bend, buckle or break easily

A

porous, less dense

88
Q

growth takes place in ________ and if these are injured it can cause ______?

A

epipheseal plates, abnormal growth

89
Q
  • A congenital abnormality in which the foot is twisted out of its normal position.
  • Muscles, tendons, and bones are involved in the abnormality.
  • adduction and supination of forefoot
  • inversion of the heel
  • fixed plantar flexion
A

clubfoot, or talipes equinovarus

90
Q

goal of care for clubfoot

A

stretch tightened ligaments and tendons gently to

Return the foot to a maximal anatomic position

91
Q
  • AKA Developmental Dysplasia of Hip
  • Abnormal development of the femoral head in the acetabulum
A

congenital dislocated hip

92
Q
  • Limited abduction of the affected hip during Ortolani maneuver. May hear a click upon movement.
  • Asymmetry of gluteal and thigh fat folds when lying with legs extended.
  • Telescoping of thigh
  • Limp and abnormal gait in older child
A

developmental displaisia of hip clinical manifestation

93
Q
  • Ensures hip flexion and abduction and does not allow hip extension or adduction.
  • It maintains correct position of the femoral head in the acetabulum.
A

Pavlik harness for developmental hip displaisia

94
Q

type of cast

A

Spica cast for developmental hip dysplasia

95
Q

type of harness for?

A

Pavlik harness for developmental dysplasia of hip

96
Q
  • Most common spinal deformity
  • Lateral curvature of spine
  • Can cause alterations in spine, chest, pelvis
  • Most frequent in girls during adolescent growth spurt
A

scoliosis

97
Q

For scoliosis treatement, a curve Less than _____ - Watch for Progression – Not Braced

A

curve less than 25%

98
Q

What is the priority psychosocial nursing diagnosis for the adolescent diagnosed with scoliosis?

A

distorted body image, could be self esteem issues

99
Q
  • Family history
  • ↑ age
  • Female
  • Menopause
  • Thin, small frame
  • Caucasian or Asian
  • Cigarette smoking
  • Excessive use of alcohol
  • ↓ calcium intake
  • Sedentary lifestyle

*risk factors for?

A

Risk factors for osteoporosis

100
Q

Osteoporosis primary

A

we don’t know what causes it, risk factors increase risk of developing it. Usually happens when aging.

101
Q

osteoporosis planning and implementation

A
  • Goal = Pain relief
  • Nursing interventions:
           - Administer analgesics, muscle relaxants, anti-                                       inflammatory med
        - Encourage use of firm mattress
        - Back brace
102
Q

secondary osteoporosis

A

can occur for a variety of reasons, usually a side effect of medications such as corticosteroids

103
Q
  • A break or disruption in the continuity of a bone
  • Risks: Trauma, Bone disease, Osteoporosis, Bone cancer
A

fractures

104
Q

Classification of fractures

A
  • Type
  • Location
  • Pattern
105
Q

preliminary dx of osteoporosis?

A

-2.5 or lower on the DEXA scan

106
Q

Recommendations for Vit D and calcium intake in people with Osteoporosis

A

1500 mg every day calcium

400-800 iu vitamin D every day

107
Q

Classification: Type

A

Classified as open or closed

108
Q

Location

A

refers to the long bones: ie: humerus, femer

109
Q

pattern

A

refers to the direction and characteristics of the fracture

110
Q

fracture physiology response

A
  • 1st 30 minutes “Local shock”: Absence of neural function
  • After 30 minutes: Pain and muscle contraction returns. Muscle spasms may cause overriding of fractured bone.
111
Q

fracture stages of healing

A
  • hematoma formation
  • cellular proliferation
  • callus formation
  • ossification
  • remodeling
112
Q
  • Deformity or shortening of extremity
  • Crepitus
  • Ecchymosis
  • Edema
  • Impaired sensation or Numbness
  • Loss of motor function
  • Loss of pulse distal to fracture
  • Pain

* clinical manifestations of?

A

fracture assessment

113
Q
  • Application of pulling force to a body part to provide reduction, alignment, and immobilization
  • Types: Skeletal, Skin, Buck’s , Pelvic, Balanced suspension
A

FracturesTraction

114
Q
  • Also called Straight or Buck’s Traction
  • Use tape, boots, splints
  • Purpose: Reduce a fracture, Decrease muscle spasms
  • Weight application: 5-10 pounds
  • Duration: 48-72 hours
A

fractures: skin traction

115
Q

type of traction?

A

skin traction

116
Q
  • Pins or wires inserted into bones
  • Purpose: Align bones and joints – “pull” on bones
  • Weight Application: 5-45 pounds
  • Duration: long term
A

skeletal traction

117
Q

type of traction?

A

skeletal traction

118
Q
  • Body part is suspended in desired position using splints, ropes, and weights
  • Purpose: Improve mobility while maintaining fracture alignment
  • Duration: Long term
  • Weight application: varies
A

Balanced suspension

119
Q

type of traction?

A

balanced suspension

120
Q

type of device?

A

external fixator

121
Q

pin care

A
  • use sterile normal saline and qtip with first pressure to circle pin site and clean around it to prevent the skin from growing up the pin (2-4 times a day)
  • sometimes paint around them with betadine or apply an antimicrobial
122
Q

4 fracture complications

A

Fat embolism
Compartment syndrome
Avascular necrosis
Infection / Osteomyelitis

123
Q
  • Fat globules lodge in pulmonary or peripheral circulation
  • Long bone fractures
  • Occurs within first 4 days
  • patho:Impaired gas exchange
    Impaired cerebral circulation
A

fractures: fat embolism syndrome

124
Q

first clinical manifestation with fat embolism syndrome

A

subtle changes in behavior and orientation

125
Q

other clinical manifestations of fat embolism syndrome

A

Seizures, focal neurologic deficits
Respiratory depression and respiratory failure
Decrease in oxygenation
Petechial rash
Substernal chest pain, dyspnea, tachypnea
Low grade fever

126
Q
  1. Increased pressure within one or more compartments causes massive compromise of circulation to the area
  2. Results in: increased circulation to muscles & nerves. Tissue hypoxia with cellular acidosis. Tissue death with loss of limb. Pain NOT relieved by pain meds
A

fracture compartment syndrome

127
Q

Increased pressure within a fascial compartment of the lower extremities or the forearm.
↓
Compression of nerves and blood vessels
↓
Nerve damage, loss of motor function and tissue ischemia

A

compartment syndrome patho

128
Q

Early signs of compartment syndrome (2)

A
  • Pain
  • Normal or decreased peripheral pulse
129
Q

late compartment syndrom s/s (5)

A
  • Cyanosis
  • Paresthesia
  • Paresis / loss of motor fx
  • Severe pain
  • Renal failure (myoglobin release
130
Q
  • An interruption in the blood supply to the bony tissue
  • Results in death of bone
  • Assessment: Pain, Decreased sensation
A

Fracture: Avascular necrosis

131
Q
  • Acute or chronic infection of bone & soft tissue
  • Usually bacterial
  • Commonly caused by Staphylococcus aureus
A

osteomyelitis

132
Q

Inflammation with recruitment of phagocytes
↓
Release of O2 free radicals and proteolytic enzymes
↓
Pus formation which impairs blood flow
↓
Ischemic necrosis of bone

A

osteomyelitis patho

133
Q
  • Local/systemic infection
  • Severe bone pain unrelieved with meds, aggravated with movement
  • Fever, chills, restlessness, malaise
  • Warmth at infection site, localized pain/ redness over the bone/ possible wound drainage
  • Elevated WBCs, erythrocyte sedimentation rate, and C-reactive protein
A

assessment for osteomyelitis

134
Q

TENS

A

-apply electrodes to skin, apply electrical impulse to nerve endings in the stump to get rid of phantom pain

135
Q
  • AKA Degenerative Joint Disease (DJD)
  • A metabolic disorder of the articular cartilage and subchondral bone of diarthrodial (synovial) joints.
  • Progressive degeneration of joints as a result of wear and tear
  • Affects weight-bearing joints
A

Osteoarthritis

136
Q
  • Age
  • May be inherited as an autosomal recessive trait
  • Excessive weight
  • Inactivity
  • Too strenuous exercise can cause secondary
  • Hormonal factors
  • Trauma
A

risk factors for osteoarthritis

137
Q

Mechanical Injury →
Chondrocyte response →
Cytokine release →
Release of proteolytic enzymes →
Erosion of bone & cartilage →
Progressive increase in micro fractures →
Decrease synovial fluid d/t degeneration of cartilage

A

osteoarthritis patho

138
Q
  • Aching that is worse with activity and relieved by rest.
  • Crepitus with movement
  • Joint enlargement
  • May involve 1 joint or many
A

osteoarthritis clinical manifestations

139
Q
  • Joint pain with movement – no pain @ rest
  • Joint stiffness after rest
  • Crepitus
  • Joint enlargement
  • Heberden nodes or Bouchard nodes
  • Unilateral joints affected
  • Limited ROM
  • Skeletal muscle atrophy
A

osteoarthritis assessment findings

140
Q
  • Tylenol
  • NSAIDs
  • Salicylates
  • Corticosteroid injections
  • Muscle relaxants
  • Magnet therapy
  • Warm moist compresses, shower
  • Paraffin dips
  • Rest / positioning
A

pain control methos for osteoarthritis

141
Q

assessment and nursing care of hip dislocation

A
  1. Assessment: Sudden severe pain
    - Lump in the buttock
    - Limb shortening
    - External rotation
  2. Nursing Care: No adduction
  • No rotation of extremity
  • No hip flexion
142
Q

3 Hip precautions

A
  • affected leg should not cross the center of the body
  • hip should not bend more than 90 degrees
  • affected leg should not turn inward
143
Q
  • Maintain drains (Hemovac, JP)
  • Maintain ice to affected joint
  • Begin CPM machine per MD order, usually 24 to 48 hrs post-op
  • Elevate affected leg
  • Avoid internal / external rotation
A

total knee replacement post-op nursing care

144
Q
  • Chronic, systemic, inflammatory autoimmune disease
  • Characterized by remission & exacerbations
  • Etiology: The definitive cause of RA is unknown. Evidence points to an immune reaction
A

Rheumatoid arthritis

145
Q
  • Persistent joint pain, even at rest
  • Morning stiffness of joints > 30 minutes to 1 hour
  • Tenderness, swelling of joints with decreased ROM
  • Joint deformities r/t instability
  • Extraarticular s/s (Systemic) = fever, fatigue , weakness, anorexia, weight loss, splenomegaly, subcutaneous nodules
  • subcutaneous nodules, swan neck
A

rheumatoid arthritis assessment

146
Q
  • Elevated erythrocyte sedimentation rate
  • Positive C-reactive protein
  • Positive antinuclear antibody test
  • Normal or mild leukocytosis
  • Anemia
  • Positive Rheumatoid factor
  • X-ray: Narrowing of joint space and erosion of articular surfaces
A

rheumatoid arthritis dx

147
Q
  • ASA and NSAIDs
  • Corticosteroids
  • Anti-rheumatic drugs
  • Antimalarial agents Immunosuppressives
  • Cytotoxic drugs
  • Heat and Cold
  • Complementary Therapies
A

pain control strategies for rheumatoid arthritis

148
Q
  • Crystal induce arthropathy
  • Primary: Innate error in metabolism → hyperuricemia
  • Secondary: Renal failure
  • Clinical manifestations: Acute attacks, chronic inflammation, tophi
A

Gout, AKA Gouty arthritis

149
Q

patho for?

A

gout patho

150
Q

Gout dx?

A

Monosodium urate crystals in synovial fluid or tophi.

151
Q
  • Autoimmune inflammatory disease causing inflammation of joints and tissue with an unknown cause.
  • Diagnosis of Exclusion: No definitive tests.
  • No Cure
  • Goals of Therapy: Control pain, preserve joint range of motion and function, minimize effect of inflammation such as joint deformity, and promote normal growth and development.
A

Juvenile Rheumatoid Arthritis (JRA)

152
Q

New treatment for Juvenile Rheumatoid Arthritis (JRA)

A

ENBREL: tumor necrosis factor (TNF) blocker that blocks the action of TNF.

BEACON MedSurg/Peds (21 decks)

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